Our lab aims to understand the mechanisms by which tumors can alter their nutrient metabolism to support their expansive growth, survival under therapeutic challenge, and metastatic potential. These changes can be promoted by genetic mutations (oncogenic activation and/or loss of tumor suppressor function), epigenetic alterations, environmental stimuli, and epitranscriptome modifications. We have previously demonstrated a direct role of the retinoblastoma protein, which was the first identified tumor suppressor, in controlling specific metabolic pathways that allow for enhanced cell proliferation as well as protection from cellular stress. Current projects, include discerning effects of altered m6A RNA modifications on hormone receptor breast cancer metabolism and alternative functions of dev novo serine synthetic enzymes. Our underlying theme in all projects is to identify specific differences within these tumor populations that can be selectively leveraged for new anti-cancer therapies.